Ion channel dysfunction has been suggested as a mechanism of peripheral nerve damage. There is a particular case in which this hypothesis is quite consistent: Oxaliplatin-Induced Peripheral Neurotoxicity (OIPN). Oxaliplatin is the cornerstone drug for colorectal cancer treatment; its use in clinical practice is limited by OIPN. There is no cure for this adverse event and it affects a vast proportion of cancer survivors. OIPN treatment has become a hot topic in Oncology practice. Transient ion channel dysfunction has been suggested to cause acute neurotoxicity symptoms: mainly, transient cold hyperalgesia, after administration (lasting 24-72 hours). A worse acute neurotoxicity has been related to a more severe chronic one (persistent sensory loss and neuropathic pain at limb extremities). Ion channels are mainly studied through in vitro techniques. However, also in vivo studies should be performed to develop new drugs for OIPN management. Our aim was implementing advanced neurophysiology in animal models to better understand OIPN pathogenesis, possibly relating acute and chronic phenomena. Nerve Excitability Testing (NET) could possibly be the solution to test axonal hyperexcitability induced by Oxaliplatin in in vivo experiments. We obtained a full NET profile of significant changes in our animal models of acute and chronic OIPN. Thus, we verified NET highly translational potential: the in vivo NET changes in animals can be matched either to findings from in vitro experiments focused on ion channels, either to clinical data (NET is easily applied in humans). We are testing AEDs to modulate acute neurotoxicity as tentative prevention of chronic OIPN

Alberti, P. (2017). Ion Channel Dysfunction and Axonal Hyperexcitability in Animal Models: a Possible Key to Peripheral Neurotoxicity. In Abstract "Festival della luce di Como - 2017".

Ion Channel Dysfunction and Axonal Hyperexcitability in Animal Models: a Possible Key to Peripheral Neurotoxicity

ALBERTI, PAOLA
2017

Abstract

Ion channel dysfunction has been suggested as a mechanism of peripheral nerve damage. There is a particular case in which this hypothesis is quite consistent: Oxaliplatin-Induced Peripheral Neurotoxicity (OIPN). Oxaliplatin is the cornerstone drug for colorectal cancer treatment; its use in clinical practice is limited by OIPN. There is no cure for this adverse event and it affects a vast proportion of cancer survivors. OIPN treatment has become a hot topic in Oncology practice. Transient ion channel dysfunction has been suggested to cause acute neurotoxicity symptoms: mainly, transient cold hyperalgesia, after administration (lasting 24-72 hours). A worse acute neurotoxicity has been related to a more severe chronic one (persistent sensory loss and neuropathic pain at limb extremities). Ion channels are mainly studied through in vitro techniques. However, also in vivo studies should be performed to develop new drugs for OIPN management. Our aim was implementing advanced neurophysiology in animal models to better understand OIPN pathogenesis, possibly relating acute and chronic phenomena. Nerve Excitability Testing (NET) could possibly be the solution to test axonal hyperexcitability induced by Oxaliplatin in in vivo experiments. We obtained a full NET profile of significant changes in our animal models of acute and chronic OIPN. Thus, we verified NET highly translational potential: the in vivo NET changes in animals can be matched either to findings from in vitro experiments focused on ion channels, either to clinical data (NET is easily applied in humans). We are testing AEDs to modulate acute neurotoxicity as tentative prevention of chronic OIPN
No
abstract + slide
Oxaliplatin, Neurotoxicity, Nerve Excitability Testing, Ion Channels
English
Festival della Luce 28 aprile-14 maggio
Alberti, P. (2017). Ion Channel Dysfunction and Axonal Hyperexcitability in Animal Models: a Possible Key to Peripheral Neurotoxicity. In Abstract "Festival della luce di Como - 2017".
Alberti, P
File in questo prodotto:
Non ci sono file associati a questo prodotto.

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/10281/152203
Citazioni
  • Scopus ND
  • ???jsp.display-item.citation.isi??? ND
Social impact